Summary Low‐temperature stress causes various types of physiological and biochemical damage to plants. The basic leucine zipper (bZIP) family transcription factor HY5 plays a significant role in multiple stress responses in plants. Here, cold stress was found to induce the upregulation of MdHY5 expression, which, in turn, positively regulates the cold tolerance of apple (Malus domestica). MdHY5 directly interacts the promoters of MdGH3‐2/12 (auxin‐amido synthetase) and inhibits their expression. However, low‐temperature stress inhibits the regulation of MdGH3‐2/12 by MdHY5, which suppresses the increase in indole‐3‐acetic acid (IAA) mediated by the MdHY5‐MdGH3‐2/12 module. Alternatively, MdHY5 directly interacts with the promoter of MdNCED2, a crucial enzyme in the biosynthesis of abscisic acid (ABA), thereby activating its expression. Additionally, cold stress enhances the regulation of MdNCED2 by MdHY5, which leads to the promotion of the increase in ABA mediated by the MdHY5‐MdNCED2 module. Therefore, under low‐temperature stress, MdHY5 reduces the ratio of IAA : ABA within apple plants by regulating MdGH3‐2/12 and MdNCED2, thereby indirectly promoting the accumulation of anthocyanins, which further improves the cold tolerance of apple. This study establishes a theoretical framework for the multiple roles and regulatory mechanisms of HY5 in integrating the IAA and ABA pathways under cold stress.

中文翻译：

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MdHY5 通过整合生长素和脱落酸途径正向调节苹果的耐寒性


总结 低温胁迫对植物造成各种类型的生理和生化损害。碱性亮氨酸拉链 （bZIP） 家族转录因子 HY5 在植物的多种胁迫反应中起重要作用。在这里，发现冷应激诱导 MdHY5 表达的上调，这反过来又正向调节苹果 （Malus domestica） 的耐寒性。MdHY5 直接与 MdGH3-2/12 （生长素-酰胺合成酶） 的启动子相互作用并抑制它们的表达。然而，低温胁迫抑制了 MdHY5 对 MdGH3-2/12 的调节，从而抑制了由 MdHY5-MdGH3-2/12 模块介导的吲哚-3-乙酸 （IAA） 的增加。或者，MdHY5 直接与 MdNCED2 的启动子相互作用，MdNCED2 是脱落酸 （ABA） 生物合成中的关键酶，从而激活其表达。此外，冷应激增强了 MdHY5 对 MdNCED2 的调节，这导致促进 MdHY5-MdNCED2 模块介导的 ABA 增加。因此，在低温胁迫下，MdHY5 通过调节 MdGH3‐2/12 和 MdNCED2 降低苹果植株内 IAA ： ABA 的比例，从而间接促进花青素的积累，进一步提高苹果的耐寒性。本研究为 HY5 在冷胁迫下整合 IAA 和 ABA 通路中的多重作用和调控机制建立了理论框架。